确定重症哮喘患者咳嗽频率与炎症标志物之间关系的观察性研究
2022/07/19
摘要
理由和目的：客观测量的咳嗽和2型生物标志物与其他哮喘控制措施和严重程度之间的关系尚不清楚。本研究的目的是评估客观和主观咳嗽测量工具与哮喘临床生物标志物之间的关系。
方法：重症哮喘和轻/中度哮喘患者完成经验证的哮喘和咳嗽相关测量工具（包括动态咳嗽监测）以及肺活量测定和T2生物标记物（呼出一氧化氮分数测量（FeNO）和外周血嗜酸性粒细胞计数（PBE））的测量。根据T2低（FeNO<20ppb和PBE<150个细胞·µl-1）、T2中间（FeNO）和T2状态对患者进行分类≥20ppb或PBE≥150个细胞·µl-1）或T2高（FeNO≥20ppb和PBE≥150个细胞·µl-1）。
结果：共有61名患者完成了研究测量（42例重度哮喘，19例轻度/中度哮喘）。在24小时总咳嗽次数（几何平均数170·3（sd 2·7）vs. 60·8（sd 4·1），p=0·002）和咳嗽频率（几何平均数7·1c·h-1（sd 2·7）vs. 2·5c·h-1（sd 4·1），p=0·002）方面，重度哮喘患者的咳嗽率高于轻/中度哮喘患者。与T2中度和T2高度哮喘患者相比，T2低重度哮喘患者24小时咳嗽频率显著降低。
结论：在T2炎症生物标志物低的患者中，咳嗽频率测量值没有升高，这表明哮喘咳嗽的机制是潜在的T2嗜酸性炎症，治疗哮喘咳嗽的合理第一步可能是用现有的治疗方法充分抑制T2炎症。
An observational study to determine the relationship between cough frequency and markers of inflammation in severe asthma
Joshua Holmes, Lorcan Pa McGarvey, Surinder S Birring, Hannah Fletcher, Liam G Heaney
Abstract
Rationale and objective：The relationship between objectively measured cough and type-2 biomarkers and other measures of asthma control and severity is poorly understood. The objective of this study was to assess the relationship between objective and subjective cough measurement tools and clinical biomarkers of asthma.
Methods：Patients with severe asthma and mild/moderate asthma completed validated asthma and cough-related measurement tools (including ambulatory cough monitoring) and measurement of spirometry and T2-biomarkers (fractional exhaled nitric oxide measurement (FeNO) and peripheral blood eosinophil count (PBE)). Patients were classified according to T2-status based on T2-low (FeNO<20ppb AND PBE<150 cells·µl-1), T2-intermediate (FeNO≥20ppb OR PBE≥150 cells·µl-1) or T2-high (FeNO≥20ppb AND PBE≥150 cells·µl-1).
Results：In total, 61 patients completed the study measurements (42 severe asthma, 19 mild/moderate asthma). Patients with severe asthma had higher rates of cough than those with mild/moderate asthma in terms of total 24-hour cough counts (geometric mean 170·3 (sd 2·7) versus 60·8 (sd 4·1), p=0·002) and cough frequency (geometric mean, 7·1 c·h-1 (sd 2·7) versus 2·5 c·h-1 (sd 4·1), p=0·002). T2-low patients with severe asthma had significantly lower 24-hour cough frequency compared to T2-intermediate and T2-high patients.
Conclusions：In patients with low biomarkers of T2 inflammation, cough frequency measurements were not elevated, suggesting that the mechanism for cough in asthma is underlying T2-eosinophilic inflammation and the logical first step for treating cough in asthma may be to achieve adequate suppression of T2 inflammation with currently available therapies.
理由和目的：客观测量的咳嗽和2型生物标志物与其他哮喘控制措施和严重程度之间的关系尚不清楚。本研究的目的是评估客观和主观咳嗽测量工具与哮喘临床生物标志物之间的关系。
方法：重症哮喘和轻/中度哮喘患者完成经验证的哮喘和咳嗽相关测量工具（包括动态咳嗽监测）以及肺活量测定和T2生物标记物（呼出一氧化氮分数测量（FeNO）和外周血嗜酸性粒细胞计数（PBE））的测量。根据T2低（FeNO<20ppb和PBE<150个细胞·µl-1）、T2中间（FeNO）和T2状态对患者进行分类≥20ppb或PBE≥150个细胞·µl-1）或T2高（FeNO≥20ppb和PBE≥150个细胞·µl-1）。
结果：共有61名患者完成了研究测量（42例重度哮喘，19例轻度/中度哮喘）。在24小时总咳嗽次数（几何平均数170·3（sd 2·7）vs. 60·8（sd 4·1），p=0·002）和咳嗽频率（几何平均数7·1c·h-1（sd 2·7）vs. 2·5c·h-1（sd 4·1），p=0·002）方面，重度哮喘患者的咳嗽率高于轻/中度哮喘患者。与T2中度和T2高度哮喘患者相比，T2低重度哮喘患者24小时咳嗽频率显著降低。
结论：在T2炎症生物标志物低的患者中，咳嗽频率测量值没有升高，这表明哮喘咳嗽的机制是潜在的T2嗜酸性炎症，治疗哮喘咳嗽的合理第一步可能是用现有的治疗方法充分抑制T2炎症。
(中日友好医院呼吸与危重症医学科 李红雯 摘译 林江涛 审校)
(Eur Respir J. 2022 Jul 1;2103205. doi: 10.1183/13993003.03205-2021.)
(Eur Respir J. 2022 Jul 1;2103205. doi: 10.1183/13993003.03205-2021.)
An observational study to determine the relationship between cough frequency and markers of inflammation in severe asthma
Joshua Holmes, Lorcan Pa McGarvey, Surinder S Birring, Hannah Fletcher, Liam G Heaney
Abstract
Rationale and objective：The relationship between objectively measured cough and type-2 biomarkers and other measures of asthma control and severity is poorly understood. The objective of this study was to assess the relationship between objective and subjective cough measurement tools and clinical biomarkers of asthma.
Methods：Patients with severe asthma and mild/moderate asthma completed validated asthma and cough-related measurement tools (including ambulatory cough monitoring) and measurement of spirometry and T2-biomarkers (fractional exhaled nitric oxide measurement (FeNO) and peripheral blood eosinophil count (PBE)). Patients were classified according to T2-status based on T2-low (FeNO<20ppb AND PBE<150 cells·µl-1), T2-intermediate (FeNO≥20ppb OR PBE≥150 cells·µl-1) or T2-high (FeNO≥20ppb AND PBE≥150 cells·µl-1).
Results：In total, 61 patients completed the study measurements (42 severe asthma, 19 mild/moderate asthma). Patients with severe asthma had higher rates of cough than those with mild/moderate asthma in terms of total 24-hour cough counts (geometric mean 170·3 (sd 2·7) versus 60·8 (sd 4·1), p=0·002) and cough frequency (geometric mean, 7·1 c·h-1 (sd 2·7) versus 2·5 c·h-1 (sd 4·1), p=0·002). T2-low patients with severe asthma had significantly lower 24-hour cough frequency compared to T2-intermediate and T2-high patients.
Conclusions：In patients with low biomarkers of T2 inflammation, cough frequency measurements were not elevated, suggesting that the mechanism for cough in asthma is underlying T2-eosinophilic inflammation and the logical first step for treating cough in asthma may be to achieve adequate suppression of T2 inflammation with currently available therapies.
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